Cytomegalovirus infection in systemic necrotizing vasculitis: causative agent or opportunistic infection?

Meyer, Martin; Hellmich, Bernhard; Kotterba, Sylvia; Schatz, H.

doi:10.1007/s002960000063

Cited by 49 publications

(33 citation statements)

References 13 publications

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“…There are a few reports to suggest that cytomegalovirus infection or reactivation may play a role in disease exacerbation, but the evidence is far from being clear [15]. In contrast, there is clear evidence that chronic nasal carriage of Staphylococcus aureus is approximately three times higher in Wegener's granulomatosis compared to healthy and disease controls and constitutes a risk factor for disease exacerbation of Wegener's granulomatosis.…”

Section: Environmental Influences: Viruses Staphylococcus Aureusmentioning

confidence: 80%

Wegener?s Granulomatosis

Lamprecht

Gross

2004

Herz

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Section: Environmental Influences: Viruses Staphylococcus Aureusmentioning

confidence: 80%

Wegener?s Granulomatosis

Lamprecht

Gross

2004

Herz

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“…Indeed, association of several genes with AAV has been previously reported (1). Bacterial and viral infections have also been implicated as environmental factors, based on clinical observations and animal models (1)(2)(3)(4).…”

mentioning

confidence: 99%

Association of killer cell immunoglobulin‐like receptor genotypes with microscopic polyangiitis

Miyashita

Tsuchiya

Yabe

et al. 2006

Arthritis & Rheumatism

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Objective. Genetic background and infection have been implicated in the etiology of microscopic polyangiitis (MPA).Although the etiology of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is poorly understood, differences in the prevalence or incidence among different populations and sporadic reports of multiplex families suggest a role of genetic predisposition. Indeed, association of several genes with AAV has been previously reported (1). Bacterial and viral infections have also been implicated as environmental factors, based on clinical observations and animal models (1-4).We previously conducted a multicenter study of the genetic background of AAV in Japan and demonstrated significant association of the HLA-DRB1*0901; DQB1*0303 haplotype with microscopic polyangiitis (MPA) (5,6). A higher incidence of MPA among Japanese patients with AAV may partly be ascribed to such a genetic background, because this haplotype is common in Asians but is rare in other populations.Killer cell immunoglobulin-like receptors (KIRs) are a diverse family of activating and inhibitory receptors expressed on human natural killer (NK) cells and a

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“…Oral cyclophosphamide and prednisone are standard treatment for PAN. However, Mayer, et al referred to the effectiveness of less aggressive treatment without immunosuppressants for immunogenic vasculitis concurrent with CMV infection [4]. Because our patient had no proteinuria, renal damage (initially), cardiomyopathy, gastrointestinal manifestations, and/or central nervous system involvement, she was also treated with corticosteroid alone without immunosuppressants, which led to partial improvement of clinical condition, such as decreasing inflammatory markers (leukocyte count, CRP and procalcitonin).…”

Section: Discussionmentioning

confidence: 83%

Dual Cytomegalovirus and Aspergillus Pneumonia Following Influenza B Infection in a Patient with Polyarteritis Nodosa

Yeh¹,

Yang²,

Yu³

2017

Int J Virol AIDS

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A 72-years-old woman of polyarteritis nodosa had fever, running nose, and nasal obstruction for 3 days. In emergency room, rapid influenza diagnostic test in nasopharyngeal swab was positive for influenza B on October 31, 2015. Chest X-ray (CXR) showed slight infiltration on bilateral lungs. A white blood cell count was 16,100/μL and an elevated C-Reactive Protein (CRP) level was 238.0 mg/L. Initial renal function was normal. Other data of laboratory testing were tabulated in Table 1.Initially, zanamivir inhalation therapy and intravenous moxifloxacin were given. However, high spiking fever was still off and on. As increased CRP (315.7 mg/L), leukocytosis (24,500/μL) and worsening dyspnea, the patient was transferred to the intensive care unit on November 09. Bilevel positive airway pressure was used for non-invasive mechanical ventilation support. Antimicrobial therapy with piperacillin-tazobactam was initiated to replace moxifloxacin. Thereafter, fever was subsided. As acute renal failure occurred, continuous venovenous hemofiltration was performed.Followed-up CXR showed newly developed consolidation over right lung fields ( Figure 1A) and the sputum cultures yielded yeast-like organisms. Antimicrobial therapy was maintained with piperacillin-tazobactam. For the therapy of PAN, intravenous methylprednisolone 40 mg every 6 hours was given since November 20, AbstractPolyarteritis Nodosa (PAN) is a systemic necrotizing vasculitis that might require immunosuppressive therapy. We report on a 72-year-old woman of PAN with influenza B infection, who developed dual cytomegalovirus and Aspergillus pneumonia in the later course. Together with steroid therapy, delayed initiation of anti-CMV and anti-fungal therapy complicated the disease course. Early diagnosis and therapy for CMV and aspergillosis in the patients post-influenza attack are important, especially in those with steroid therapy.

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Cytomegalovirus infection in systemic necrotizing vasculitis: causative agent or opportunistic infection?

Cited by 49 publications

References 13 publications

Wegener?s Granulomatosis

Wegener?s Granulomatosis

Association of killer cell immunoglobulin‐like receptor genotypes with microscopic polyangiitis

Dual Cytomegalovirus and Aspergillus Pneumonia Following Influenza B Infection in a Patient with Polyarteritis Nodosa

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